Bicarbonate modulates oxidative and functional damage in ischemia-reperfusion

Free Radic Biol Med. 2013 Feb:55:46-53. doi: 10.1016/j.freeradbiomed.2012.11.007. Epub 2012 Nov 27.

Abstract

The carbon dioxide/bicarbonate (CO(2)/HCO(3)(-)) pair is the main biological pH buffer. However, its influence on biological processes, and in particular redox processes, is still poorly explored. Here we study the effect of CO(2)/HCO(3)(-) on ischemic injury in three distinct models (cardiac HL-1 cells, perfused rat heart, and Caenorhabditis elegans). We found that, although various concentrations of CO(2)/HCO(3)(-) do not affect function under basal conditions, ischemia-reperfusion or similar insults in the presence of higher CO(2)/HCO(3)(-) resulted in greater functional loss associated with higher oxidative damage in all models. Because the effect of CO(2)/HCO(3)(-) was observed in all models tested, we believe this buffer is an important determinant of oxidative damage after ischemia-reperfusion.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bicarbonates / metabolism*
  • Bicarbonates / pharmacology
  • Buffers
  • Caenorhabditis elegans / drug effects
  • Caenorhabditis elegans / metabolism*
  • Carbon Dioxide / metabolism
  • Cell Survival / drug effects
  • Cells, Cultured
  • Disease Models, Animal
  • Heart
  • Hydrogen-Ion Concentration
  • Male
  • Mice
  • Oxidation-Reduction / drug effects
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / metabolism*
  • Reperfusion Injury / pathology

Substances

  • Bicarbonates
  • Buffers
  • Carbon Dioxide